Chest trauma

Pulmonary trauma

• Blunt thoracic trauma = ¼ of all trauma-related deaths
• Those penetrating trauma who survive to hospital generally have better outcomes than those with blunt trauma
• Penetrating chest injuries in cardiac box (bound by sternal notch, xiphisternum and both nipples)
  • = Cardiac or great vessels until proven otherwise

• Examination
  • Distended neck veins may indicate tension PTX, cardiac tamponade, cardiac failure or air embolism (need sufficient blood volume though)
  • Plethoric/cyanotic/swollen neck and face may suggest SVC obstruction and severe superior mediastinal injury
  • Scaphoid abdomen suggests diaphragmatic injury
  • If unilateral breath sounds consider mainstem bronchus intubation (>23cm in adult males or 21cm in adult females), pneumothorax or haemothorax
  • Palpation of chest with patient coughing may yield more subtle fractures
  • Sensitivity of auscultation for haemothorax is 50%

• Imaging
  • CXR
    • Up to 50% of patients with blunt chest trauma have normal CXR with subsequent multiple injuries on CT (not all change management however)
  • Ultrasound
    • Greater sensitivity and equal specificity than CXR for haemothorax
    • Sensitivity 92% with near 100% specificity for pneumothorax (vs. 50-80% sensitivity and 90% specificity for plain films)
    • US in the ED can detect occult PTX as accurately as CT
  • CT
    • More sensitive for pulmonary contusion and haemothorax than CXR

• NEXUS chest rules
  • For blunt trauma patients only >14yo
  • If any of the below, need CXR:
    • Age >60
    • Rapid deceleration (fall 6m, MVA >64km/hr)
    • Chest pain
    • Intoxication
    • Abnormal alertness
    • Distracting painful injury
    • Tenderness to chest wall palpation
  • 98.8% sensitivity and 13.3% specificity (only half went on to get CT limiting comparisons)

• Oesophageal injury
  • Requires water-soluble contrast orally if high suspicion
  • Barium swallow may cause mediastinitis (but has few false positives)
• Initial resuscitation
  • Maintaining adequate ventilation and oxygenation in the acute chest trauma patient is critical
  • If respiratory distress is not immediately remedied by specific intervention, I&V
  • VBG/ABG is very helpful – Metabolic acidosis with insufficient ventilatory compensation is an indication for ventilatory support measures

• Cardiac arrest associated with intubation
  • Inadequate pre-oxygenation
  • Oesophageal intubation
  • Intubation of right or left mainstem bronchus
  • Tension pneumothorax
  • Systemic air embolism
  • Decreased venous return due to excessive ventilatory pressure/rate
  • Vasovagal response
• Unexplained bradycardia should prompt immediate verification of tube placement, exclusion of oesophageal placement and evaluation for tension pneumothorax

• DOPES mnemonic for post-intubation hypoxia
  • Displacement of ET
  • Obstruction of ET
  • Patient – Pneumothorax, PE, bronchospasm, APO, collapse
  • Equipment – Ventilator issues
  • Stacked breaths – Bronchospasm and incorrect ventilator settings
• Steps
  • Disconnect ventilator and bag on 100% O2
  • MASH approach patient assessment
    • Movement of chest wall 
    • Arterial saturation
    • Skin colour
    • Haemodynamic stability
  • If little chest movement
    • Rule out ET issue – displacement, obstruction, consider CXR, may have to remove tube
  • If chest wall moving but desaturating
    • Patient problem more likely – PTX, lung collapse, APO, bronchospasm, APO

Tension pneumothorax

• Classic presentation
  • Unilateral breath sounds, tracheal deviation, distended neck veins, hypotension
• 14G cannula to 2^nd ICS in MCL
  • Avoid internal mammary vessels (3cm from sternal border)
  • Avoids mediastinal vessels
  • Shortest distance to pleura
• Alternative site is 4^th/5^th ICS in anterior axillary line (as for ICC)
• Follow with tube thoracostomy

Massive haemothorax

• Common causes
  • Injury to lung parenchyma, intercostal arteries, internal mammary arteries
• Each hemithorax can hold 40% of blood volume
• Defined as >1500mL in adult or 2/3 of hemithorax
• Life-threatening by three mechanisms
  • Hypovolaemia
  • Hypoxia due to collapsed lung, VQ mismatch, anatomic shunting
  • Tension obstructive shock
• Suggested by reduced breath sounds, dullness to percussion and no chest wall movement
• Collapsed lung due to contralateral mainstem intubation can mimic haemothorax and must be ruled out before ICC placement

Open pneumothorax

• Respiratory distress results due to lung collapse and inability to ventilate the affected lung
• Air entry reduced on affected side with impaired chest wall rise
• Sucking chest wound usually apparent
• Cover wound with 3-sided dressing to act as valve
  • Complete occlusion results in tension PTX
• Do not place subsequent ICC through wound as may follow tract into lung/mediastinum/diaphragm

Systemic air embolism

• Disastrous circulatory and neurological collapse
• Risk in those with penetrating chest wound with PPV ESPECIALLY if haemoptysis evident
• High PPV (>50cmH20) may force air from injured bronchus into circulation as pressures exceed venous pressure
• If suspected
  • Place in supine position with 100% oxygen applied (may allow nitrogen reabsorption)
  • No evidence for head down position in arterial air embolism
  • Hyperbaric oxygen therapy helps to reduced size and increase resorption of air bubbles
• To prevent this, consider single lung ventilation in patients at high risk
• In the event of arrest or peri-arrest situation:
  • CPR and immediate thoracotomy to clamp affected lung area followed by air aspiration from heart and ascending aorta
  • Open cardiac massage with clamping of the ascending aorta may help to push air through coronary arteries
  • Initiate coronary artery bypass promptly if available

Tube thoracostomy

• Evacuate large haemo/pneumothoraces as soon as possible to minimise effects of ventilation and perfusion
• Double-check imaging to ensure correct side
• 24Fr or Seldinger recommended for simple pneumothorax
• One study showed no differences in efficacy, complication rate, pain or need for further procedures with small or large tubes

• Insertion site
  • Anterior axillary line at 5^th ICS
• Make incision 1-2cm below this to allow oblique passage and subsequent easy closure and reduced risk of recurrent PTX with tube removal
• Blunt dissect in layers using curved forceps down to pleura then through and dilate
• Check with finger that lung not adhered to chest wall and that you are in fact in pleural cavity
• Never leave tract with nothing in it as easy to lose
• Advance tube through hole until last side hole is 2.5-5cm into chest wall
  • For pneumothorax, direct to apex
  • For haemothorax direct posteroinferiorly
  • Directing is made easier if forceps are inserted into most distal eyelet and turned in the chest (this does however mean instrumenting the thoracic cavity, which some authors make all attempts to avoid)
  • Can also try to direct using your finger but can be less effective
  • If tube is simply inserted with no direction, often ends up in fissure (and thus is made less effective)
• Secure
  • 0-silk used
  • Place tube at base of incision, make large bites just above the tube either side to close the wound tightly around tube
  • Cut off sharp
  • Hand- or instrument-tie the skin closed leaving 10-15cm loose end and longer end to secure around the tube
  • Make hitch knots with one end of the suture around tube repeatedly 5-6 times then tie off using other loose end of suture

• In general, do not clamp for any reason
  • Any continued air leakage can cause rapid tension PTX or lung deflation
• Deterioration after placement may indicate exsanguinating injury and loss of tamponade effect. In this circumstance, clamp and get urgent thoracotomy (in ED if peri/arrest)
• Attach to underwater seal mechanism and -20cmH20 of suction
  • Suction is set on the Atrium Drain with a built-in dial while wall suction must be set at ~100mmHg
  • While on suction, swinging will not be apparent but bubbling will continue if there is a persistent pneumothorax or air leak
• Document placement and function
• CXR to confirm placement and last hole in chest wall
• If obstructs, place another rather than flush
• Leave in place for 24 hours after air leak ceased (no further bubbling) or until serous and <200mL/24 hours if haemothorax) or until extubated (if on PPV)
• Prophylactic antibiotic use remains controversial (not routine in Aus)

Troubleshooting chest drains

• Clamping
  • Clamp ICC on insertion to prevent leakage of fluid, connect to drainage system and then unclamp
  • Otherwise should only clamp for very specific reasons:
    • Briefly when changing drainage system
    • If positioning cannister above patient for any reason (briefly)
    • Massive haemothorax under Cardiothoracic direction as a temporising measure to tamponade bleeding
  • Should never clamp a drain for a pneumothorax while on positive pressure ventilation
  • Do NOT clamp chest tubes for transport
  • Clamping trials are sometimes done prior to removal if a pneumothorax is thought to have resolved under medical guidance
• Re-expansion pulmonary oedema
  • Classically presents as SOB, cough, shoulder tip pain after >1.5L per hour removal of pleural fluid
  • Ideally should aim for <1-1.5L per hour using clamping to slow the drainage rate
• Air leak
  • Bubbling is evidence of air leak
  • A sudden large volume air leak (constant and reaching 4/5 on scale of Atrium cannister) suggests a bronchopleural fistula OR disconnected/loose system OR displaced pleural catheter out of thoracic cavity
  • Ongoing small air leak suggests pneumothorax still remains and lung has not fully re-expanded
  • Sudden cessation of air leak suggests:
    • Lung re-expansion
    • Occlusion/obstruction of tube
• Swinging/tidal
  • If NOT on suction, should see tidal swinging of ball and fluid representing negative pressure ventilation transmitted through the drainage system
  • If on suction, this will not be present
  • If suddenly ceases and NOT on suction, this represents:
    • Obstruction
    • Kinking
    • Malposition out of thoracic cavity
  • If suspicious that tube may have become obstructed or displaced, can cease suction to check for swinging periodically
• Tube falls out
  • Redress site with vaseline-impregnated gauze and either occlusive dressing for pleural fluid/haemothorax OR three-sided dressing for pneumothorax
  • Decide whether ICC needs to be reinserted
• Drainage system disconnection
  • Clamp close to patient
  • Reconnect to new drainage system
  • Unclamp

ETT as alternative to ICC

• Beer et al. (2010) in a small study showed equal efficacy and reduced time to insertion between these two methods
• Queensland Ambulance Service currently recommends 7.0 ETT insertion through finger thoracostomy utilising a Cook intubating catheter in obese finger thoracostomies and/or 2 or more re-finger decompressions
• Thought to be faster (no suturing), as effective and easy to connect to either Heimlich valve/Cook ICC valve or drainage bag for closed circuit
• May be useful in ED when unstable patient with finger thoracostomy/s requires urgent imaging and formalisation with ICC would take too long – acts as temporising measure

Pulmonary contusion

• Definition: Direct injury to lung resulting in haemorrhage and oedema in the absence of pulmonary laceration
• Most common cause is compression-decompression mechanism, such as high-speed MVA
• Two stages
  • First-stage is direct lung injury
  • Second-stage is resuscitative measures (particularly crystalloid resus)
  • Self-perpetuating as unaffected lung receives full brunt of right heart output with subsequent interstitial oedema/dysfunction and then moves onto the next healthy segment
  • Leads to intrapulmonary shunting, resistance to airflow, decreased lung compliance, increased WOB, hypoxia, hypercarbia, acidosis and decompensation

• May have decreased or coarse breath sounds over region
• CXR and CT show patchy, ground-glass opacification and widespread consolidation in severe cases
• Contusions cross segments and across pleural fissures
• Areas of consolidation seen within 6 hours of injury are considered diagnostic of pulmonary contusion (vs. aspiration pneumonia or fat embolism – radiological findings delayed)
• CT far more sensitive (70% not seen on initial CXR)
  • Also helps prognosticate. If >20% lung volume involvement = 80% risk of ARDS/ALI

• Treatment
  • Maintenance of adequate oxygenation/ventilation and pain control
  • Epidural analgesia/intercostal blocks/paravertebral analgesia are all good options
  • <25% (<1 lobe) involvement usually do not require mechanical ventilation
  • Avoid excessive fluid administration
  • NIV should be considered and trialled if support indicated
  • Steroids are contraindicated
  • Place non-injured lung dependent if mechanical ventilation utilised to improve VQ matching
  • Single lung ventilation may be assistance as may high frequency oscillation ventilation (although no clear survival benefit)
  • Diuretics may be used if hypervolaemic and if not contraindicated by haemodynamic instability

Haemothorax

• Most commonly due to bleeding from direct lung injury
• Limited by compressive effect of lung, high lung thromboplastin concentration and low PAP
• Bleeding of venous origin usually tamponades without intervention
• Damage to intercostal, internal mammary arteries or pulmonary vessels almost always requires invasive management
• EAST guidelines state all haemothoraces, regardless of size, should have drainage considered
• No clear guidance on management of occult (visible on CT only) or non-significant (<2cm)
• Gilbert et al. looked at 6 studies and 1400 patients with occult haemothoraces (visible on CT, not on initial CXR)
  • Found failure rate of expectant management of 23%
  • Of the 23% of failures that gave a reason, 73% were for progression of haemothorax, 18% for worsening respiratory status and 8% progression of pneumothorax
  • Patient age, higher ISS and presence of pneumothorax were not predictive of failure of expectant management
  • Haemothorax size >300mL increased OR of failure by 3.02
  • Need for mechanical ventilation predicted failure of expectant management
  • There was no mortality difference between expectant and initial tube thoracostomy
  • The empyema rate was 6% in the tube group vs. 0% of expectant
  • Unclear whether expectant management of occult haemothorax <300mL (<1.5cm max depth on CT) is safe and needs further study
• Evacuate haemothoraces >300mL expeditiously to avoid complications
  • Large clots in the pleural space can act as anticoagulants through release of fibrinolysins
  • Bleeding from multiple small intrathoracic vessels usually stops rapidly after haemothorax is evacuated
• Fluid collections >200mL can be seen on upright or decubitus CXR
  • >1000mL can be missed if supine film (get diffuse haziness only)
    • POC USS may be useful in this scenario if too unstable for CT
    • CT has highest sensitivity and specificity

• Indications for operative intervention
  • Consider if:
    • >1500mL evacuated immediately after tube thoracostomy
    • >150-200mL/hr for 2-4 hours
    • Persistent blood transfusion required to maintain haemodynamic stability
• <5% of patients with blunt chest trauma require tube thoracostomy let alone operative intervention

Traumatic Pneumothorax

• Best seen on upright CXR upper lateral region
  • Avoid interpreting scapula or skin folds as pneumothoraces
  • POC USS far superior if supine and CT even better
• Seen in 20% of patients with significant chest trauma
• If previously well, usually no significant symptoms until >40% of hemithorax involved
• Occult pneumothoraces can complicate subsequent operative interventions due to initiation of PPV and conversion to large/tension PTX
• Patients with COPD or airway obstruction are at higher risk of forcing more air into pneumothoraces in expiration leading to tension
• Plain film will miss 17% of PTX if erect and 80% if supine
• Occult pneumothoraces are those detected by CT but not seen on CXR
• Pneumothorax after a stab wound can be delayed up to 6 hours
  • Therefore repeat imaging is indicated at this time point or if any deterioration occurs
  • There is a 12% incidence of delayed pneumo/haemothorax in initially stable chest stab victims
  • If repeat CXR is normal at 4-6 hours, often can discharge if asymptomatic

• Treatment
  • If cannot be observed closely, moderate-large size, enlarging, PPV initiated/required or will be transported long –distance by any means (especially by air) insert a chest tube or pigtail
  • Small pneumothoraces (<1cm wide, confined to upper third of chest)
    • If unchanged on two CXR taken 4-6 hours apart in otherwise well individuals can be treated by observation alone
  • Occult pneumothoraces
    • Observation alone unless patient requires mechanical ventilation
    • EAST guidelines state can still be managed conservatively but need to monitor closely
  • 22% risk of major insertional, positional and infective complications with intercostal catheters so AVOID if possible
  • Small- or moderate-sized PTX, once treated, do not cause problems unless continuing air leak or underlying cardiopulmonary disease
    • Small air leaks usually don’t cause any issues, provided lung is fully expanded
    • Empyema and bronchopleural fistulas are greatly increased if continued air leak persists >24-48 hours
• Walker et al. 2017
  • 602 pneumothoraces -> 325 chest intervention + 277 conservative
  • 25 Failed conservative Mx
  • Those managed conservatively had significantly smaller (5.5mm vs 22mm) with majority <10mm
  • No significant difference in failure rate between conservatively managed patients on PPV and those not on PPV
  • On univariate analysis, size of pneumothorax, MOI, rib fractures, clinical condition, surgery and ISS were not significantly associated with failure of conservative Mx
    • Although in conservative arm, 5.3mm vs. 8.2mm (so mostly small)
  • The presence of haemothorax >2cm was associated with a much higher likelihood of failed conservative management (HR 4.08)

• Troubleshooting
  • If lung does not completely inflate or persistent airleak consider:
    • Improper connections
    • Improper positioning of tube
    • Occlusion of bronchi/bronchioles
    • Tear of a larger bronchus
    • Large tear of lung parenchyma
  • If PTX persists or large air leak, perform urgent bronchoscopy to examine and clear the bronchi OR to identify and repair any damage to the tracheobronchial tree
  • Early thoracotomy is indicated if this continues despite above measures

Pneumomediastinum

• Indicated by subcutaneous emphysema in neck or crunching sound (Hamman’s sign) over heart during systole
• Diagnosis on CXR or CT
• In blunt chest trauma:
  • Usually alveolar rupture, followed by dissection along bronchoalveolar sheath and spread of air into mediastinum (Macklin effect)
  • Can be asymptomatic or cause chest pain, SOB, voice change, cough or stridor
  • Only need intervention if symptomatic, in which case need to search for injuries to larynx, trachea, major bronchi, pharynx and oesophagus
• On CXR can see as clear diaphragm all the way across the mediastinum
• On CT may see pulmonary interstitial emphysema (Macklin effect) which is fairly definitive in showing the source of the air leak as coming from the lungs rather than oesophagus

Pulmonary haematoma

• Parenchymal tears filled with blood
• Usually resolve spontaneously over weeks
• Risk of infection and lung abscess
  • More likely if intubated+ventilated, prolonged chest tube drainage or post-thoracotomy

Pulmonary laceration with haemopneumothorax

• Mostly seen with displaced rib fractures due to direct trauma
• Lung laceration appears as traumatic pneumatocoeles rather than a linear tract
• Haemorrhage can also occur from shear forces on preexisting pleural adhesions during rapid deceleration or penetrating chest injuries

Intrabronchial bleeding

• Can lead to severe hypoxaemia and rapid death
• Hinders gas exchange like drowning
• It is crucial to identify involved lung and isolate it
  • Bronchoscopy is often necessary to identify injury and control haemorrhage
• Intubation with frequent tracheal suctioning may be effective
• If haemorrhage severe, double-lumen tube to confine bleeding to one lung as a temporising measure is indicated
  • Or can purposely pass single lumen ET into unaffected lung or 
  • Purposely intubate right mainstem bronchus as diagnostic measure, see if blood suctioned up and place affected lung in dependent position with retraction of ET to normal position after this

Aspiration

• Common after severe trauma
• CXR changes often delayed up to 24 hours
• Right middle and lower lung fields most commonly affected
• Frequent suctioning and reassessment is key
• No evidence for prophylactic antibiotics until confirmed aspiration pneumonia

Injuries to trachea and major bronchi

• Mainly rapid deceleration injuries causing shear forces on more mobile distal airways
• Forced expiration against closed glottis and compressive force can also lead to this
• Most occur within 2cm of carina or at origin of lobar bronchi
• Presentation
  • Dyspnoea, haemoptysis, subcutaneous emphysema, Hamman’s sign and sternal tenderness
  • Large PTX, pneumomediastinum, deep cervical emphysema also suggest this
  • 10% have mild or no symptoms

• The air leak following thoracostomy is continuous and massive in the setting of bronchopleural fistula
  • High-frequency oscillation is the ventilatory method of choice until repair
  • All lacerations >1/3 diameter of bronchus need surgical repair
  • Untreated tracheal tears risk mediastinitis or severe bronchial stenosis with atelectasis and recurrent pulmonary infection
• Concurrent oesophageal injuries occur in 25% of penetrating tracheobronchial injuries and are easily missed unless water-soluble contrast oesophageal swallow study or upper GI scope performed
• Intrathoracic tracheal transection is almost invariably fatal. Those that survive to hospital usually have cervical tracheal transection only

Cervical tracheal injuries

• Usually found at jx of trachea and cricoid cartilage
• Most often anterior neck strikes steering wheel or dashboard
• Subcut emphysema, stridor and bruising should raise suspicion
  • Consider associated spinal and vascular injuries

Diaphragmatic injury

• Most commonly due to penetrating trauma between umbilicus and nipple line
• Rupture due to blunt trauma is far less common (<5% of hospitalised blunt trauma patients)
  • Fracture of pelvis increases risk of this (10-15% of pelvic trauma patients)
• Left sided predominance in blunt trauma due to liver protection on right and possible vulnerable posterolateral left diaphragm – although latest data shows equal L:R
• Delayed presentation unless defect is very large
  • Diaphragmatic herniation of intestines can take years
  • At its worst can cause tension enterothorax or bowel infarction/obstruction
• CXR shows findings in only 25% of cases (deAlwis state most have at least one non-specific finding)
• Diagnostic tests include:
  • CT (still not 100%)
  • Orogastric placement to see if curls back up into chest from stomach
  • Upper GI series
  • Thoracotomy or laparotomy often required if suspicion remains after CT
• Treatment
  • NG to decompress + ICC in usual spot carefully placed if haemo/pneumothorax

Oesophageal injury

• Most commonly direct penetrating trauma with high mortality
• If suspected, perform water-soluble contrast oesophagogram
  • Recommended to repeat with barium swallow if negative due to high false-negative rate
• Flexible oesophagoscopy may miss some injuries, even when combined with an oesophagogram
• Some surgeons prefer rigid oesophagoscopy combined with bronchoscopy to rule out associated tracheobronchial injuries
• Contrast studies do NOT interfere with later oesophagoscopy

Thoracic duct injuries

• Consider in penetrating trauma near the left proximal subclavian vein
• Development of chylothorax has a mortality rate of 50% and should be considered in all chest trauma patients

Subcutaneous emphysema

• Usually occurs as air from lungs or tracheobronchial tree gains access to chest wall through defect in parietal pleura
• Can also dissect from interstitial lung injury back along the bronchi into the hilum and mediastinum and then into the extrapleural spaces
• If extensive, suggests injury to major bronchi, pharynx, larynx or oesophagus
  • Requires bronchoscopy +- oesophagoscopy
• Assume there is an underlying pneumothorax in all cases and if PPV is required, insert a chest tube on the involved side

Rib fractures

• Diagnosed in 50% of admitted patients following chest trauma
• Closely associated with morbidity and mortality
• Must rule out associated haemothorax, pneumothorax, lung contusion, intra-abdominal injury or major vascular injury
• If significantly displaced rib fractures or severe chest injury, serial radiography is necessary to monitor for delayed complications
• Up to 50% not apparent on plain films (esp. anterolateral of first 5 ribs)
• Injuries to cartilagenous portions may never be apparent on radiographs
• US is a promising option for diagnosis of both bony and cartilagenous defects

• First 2 ribs
  • Takes great force or direct trauma to fracture these
  • Can be associated with blunt myocardial injury, bronchial tears or major vascular injuries
  • 15-30% have poor outcomes (usually head injury or major vessel disruption)
• If multiple fractured ribs (esp. 9, 10, 11), unexplained hypotension has to be assumed to be from intra-abdominal injury (splenic or liver bleed)
  • Multiple rib fractures often cause inadequate ventilation and coughing and warrant a period of observation, especially if elderly or comorbid illness

• For mild to moderate chest wall pain:
  • Combination opioids, benzodiazepines, topical lignocaine patch and NSAID’s provide the most effective analgesia regime to allow adequate ventilation and prevent atelectasis/pneumonia
  • Intercostal nerve blocks with bupivacaine can ease pain for up to 12 hours
  • Epidural analgesia and intrapleural catheters for local anaesthetic instillation are also effective

Flail chest

• Segmental fractures of 3 or more adjacent ribs anteriorly or laterally can result in clinical flail chest
  • Paradoxical inward movement of segment during inspiration and outward movement on expiration
  • Can greatly increase the work of breathing BUT hypoxaemia often due to underlying pulmonary contusion
  • May fatigue rapidly with vicious circle of decreasing ventilation, increasing WOB and hypoxaemia with subsequent respiratory arrest
• If mild to moderate flail chest, minimal underlying lung damage and no associated injuries can often be managed without mechanical ventilation
  • Need adequate analgesia including intercostal blocks and maintaining good ventilation (incl. NIV) and pulmonary toilet
• If underlying lung contusion, far more likely to require mechanical ventilatory support

• Indications for early ventilatory support:
  • Shock
  • Severe head injury
  • Comorbid pulmonary  disease
  • Fracture of 8 or more ribs
  • Associated injuries
  • Age >65
  • PaO2 <80 despite supplemental oxygen
• Early intubation and ventilation has improved mortality outcomes compared to delayed intubation until onset of respiratory failure
• Consider surgical fixation in patients requiring mechanical ventilation when thoracotomy is performed for other reasons

Sternum fracture

• Lateral chest x-ray may show fracture however CT and USS are more sensitive
• If isolated sternal fracture and otherwise negative workup can often be discharged home.
  • Requirements:
    • Otherwise normal chest CT
    • Normal echo
    • Normal cardiac enzymes at time of presentation and 6 hours later (??)
    • Normal ECG at presentation and 6 hours later
• Previously thought to correlate with high risk of mediastinal injuries however, only 1.5% incidence of arrhythmias and 1% mortality
• Seems from this data that isolated sternal fractures are NOT a clear indicator of underlying blunt myocardial injury

Traumatic asphyxia

• Sudden, severe crush injury to the chest can cause subconjunctival haemorrhage, petechiae, vascular engorgement, facial oedema and cyanosis of the head and neck
• Likely due to abrupt sustained rise in SVC pressure with concurrent closure of the airway after deep inspiration
• Neurological impairment, if evident, is often temporary and long-term morbidity is primarily related to associated injuries

Cardiac trauma

• Penetrating cardiothoracic trauma causes 25% of deaths following trauma
  • Majority due to cardiac or great vessel injury
• Cardiac injury accounts for 10% of deaths following gunshot wounds
• Incidence of blunt cardiac injury following major trauma is estimated at 8-71%
• Suspect cardiac or great vessel trauma in any patient with chest, lower neck, epigastric or praecordial injury
• Closely observe for haemodynamic instability, hypovolaemia, dysrhythmias, tamponade and haemothorax

Penetrating cardiac trauma

• Rates of involvement of cardiac structures
  • RV 40% (large anterior exposure)
  • LV 35%
  • RA 20%
  • LA 5%
• Stab wounds 17x more likely to survive than gunshot wounds to the heart
• Anatomical cardiac box
  • Xiphisternum to sternal notch and across to each nipple
  • Stab wounds tend to enter in this region but gunshot wounds can enter anywhere
• Cardiac tamponade and exsanguinating haemorrhage are the two most common conditions seen after penetrating trauma
• Pericardial linear lacerations tend to close themselves leading to tamponade
• RV lacerations tend to seal themselves more readily than RA wounds due to thicker, more muscular wall
• Atrial injuries are often subtle and may be initially asymptomatic with subsequent haemodynamic collapse
• Injury to the coronary arteries presents with tamponade or myocardial ischaemia

Cardiac tamponade

• Seen in 2% of penetrating trauma to the thoracoabdominal region and very rarely in blunt trauma
• 80% of myocardial stab wounds will result in tamponade
• Gunshot wounds are less likely to cause tamponade due to large defects
• Blood in the pericardium may be defibrinated by lytic activity normally present, resulting in enlarging haematoma inhibiting normal myocardial function and ultimate tamponade physiology
• Release of catecholamines due to impaired CO results in ever increasing right sided heart pressures, septum moves across to left and LV filling is impaired even further
• Even 65-100mL can lead to an acute rise in intrapericardial pressure
• Hypovolaemic shock from other injuries can result in low or normal central venous pressure, making diagnosis more difficult

• FAST scan is critical
• Diagnosis is made more difficult by compensatory tachycardia, rise in SVR and hypovolaemia from other causes
• Beck’s triad (muffled HS, hypotension, distended neck veins) evident in only 10%
• Pulsus paradoxus (substantial fall in SBP during inspiration) and Kussmaul sign (raised JVP on inspiration) are not reliable and may only be evident with moderate to severe tamponade
• Narrowed pulse pressure with elevation of central venous pressure is tamponade until proven otherwise (more reliable than above)
  • Narrowed pulse pressure is not sensitive so if absent, cannot rule out tamponade

Intracardiac missiles

• Can be direct trauma or venous migration from another injury
• The missile +- thrombus can then embolise to pulmonary or systemic arteries
• Can be treated conservatively or removed
• Indications for removal
  • Haemodynamic instability or symptoms
  • An LV missile that is free or partially exposed should be removed to prevent systemic embolisation
  • Embolised missiles
  • Embedded or adjacant to coronary artery
• Right sided missiles can be either removed or left in situ because embolisation to the pulmonary vessels is usually of minimal consequence
• Most intramyocardial or intrapericardial missiles are left in situ with observation
• Long-term effects of conservative treatment can include bacterial endocarditis, thrombosis, embolisation and cardiac neurosis (obsession with object and symptoms)

Pericardiocentesis

• Performed if clinical tamponade diagnosed and there is a delay to theatre for thoracotomy
• Rarely indicated for traumatic pericardial effusion/haemorrhage

ED Thoracotomy

• Performed in unstable patients with cardiac tamponade who may not survive transport to theatre
• Indicated if haemodynamically unstable or arrests and demonstrate signs of life after penetrating trauma in the field or ED (or in the ED following blunt trauma)
• Likely to be futile if no pulse or BP in field, asystole is presenting rhythm and no tamponade, prolonged pulselessness >15 minutes at any time, other non-survivable injuries or blunt traumatic cardiac arrest
• Do not put digit through any defect. Simple digital occlusion is the first step and can then staple shut myocardial defects using skin staples
• Survival rate for patients that make it to the operating theatre is 70-80% for stab wounds and 30-40% for gunshot wounds

Blunt cardiac trauma

• Up to 20% of MVA deaths are due to blunt cardiac injury
• Mechanisms
  • Shearing forces from rapid deceleration or torsion causing tear in heart at point of fixation (RA and vena cava) – rapid deceleration is most common mechanism followed by direct praecordial impact
  • Direct praecordial impact
  • Crush injury from compression
  • Abrupt pressure fluctuations in chest and abdomen
  • Injury from rib fracture segments
  • Hydraulic effect resulting in cardiac rupture
  • Blast injury

• Encompasses myocardial dysfunction, dysrhythmias, specific injuries (e.g. septal rupture) and cardiac rupture
• Most often involves right heart as lies anteriorly (with minimal ECG changes)
• More than one chamber involved in >50% of cases
• Minor troponin leaks, ECG abnormalities and dyskinesia/dysrhythmias usually resolve over 24 hours
• Injuries that lead to death include complex dysrhythmias, acute heart failure, free wall rupture or coronary artery laceration
  • Typically cause death at scene
• Less severe injuries to the free wall can cause delayed necrosis and rupture
• If low-pressure chamber or coronary vein is injured, may survive to hospital
• Can also result in shunt across septal defect, papillary muscle failure, valvular failure, which all tend to present later with heart failure symptoms

Commotio cordis

• ’Disturbance of the heart’
• Sudden death due to blunt trauma to chest wall
• 2^nd most common cause of death in young athletes after HOCM
• Highest incidence in baseball/hockey.etc.
• Usually low impact with no other associated injuries
• Primary electrical event with induction of VF due to blow occuring 10-20ms before peak of T wave (vulnerable period)
• Overall survival rate <15% but AED at sporting fields may improve this

Associated injuries

• Chest pain is universal but often due to concomitant chest wall injuries
  • Rib fracture (up to 70%)
  • Aortic or great vessel injury (20-40%)
  • Haemothorax (up to 65%)
  • Pulmonary contusion (up to 60%)
  • Pneumothorax (up to 40%)
  • Flail chest (up to 40%)
  • Sternal fracture (up to 60%)
• Head injury seen in up to 73%
• Extremity injury in up to 66%
• Abdominal solid organ injury in up to 43%
• Spinal injury in 10-20%

Cardiac dysfunction

• Persistent tachycardia, new BBB, ST, AF, VF and occasional PVC’s can all be an indicator of blunt injury
• There is a lack of consensus on definition of ‘myocardial contusion’
• Often manifests on echo as diminished contractility, decreased CO and low MAP
• Many changes resolve within 24 hours

Arrhythmia

• Assume haemorrhage is cause of tachycardia until proven otherwise
• Unexplained persistent tachycardia, new BBB and minor arrhythmias (occasional PVC’s) raise suspicion of BCI
  • Patients with any of these findings should be admitted for observation

Concomitant injury and sternal fracture

• Sternal fracture DOES NOT imply presence of BCI (particularly if only visible on CT)
• BCI rarely occurs in isolated sternal fracture
• Presence of sternal fracture NOT associated with increased mortality

Pericardial injury

• Can be due to direct impact or raised intraabdominal pressure causing a tear
  • Usually left side parallel to phrenic nerve
  • Herniation can occur through the defect with subsequent cardiac dysfunction or dysrhythmias
• Often missed
• Pneumopericardium appears as a smooth spherical air-filled cavity vs pneumomediastinum where bubbles track everywhere
• May be evident by pericardial rub, POCUS, CT (pneumopericardium, bowel gas in chest)
• Usually taken to the operative theatre for repair unless so large that tension across repair would impair myocardial function

Injury to valves/papillary/septum/
chordae tendinate

• Valve injuries occur in 10% of blunt cardiac injuries
• Aortic most commonly
  • Can get immediate regurgitation and APO
• Suspect if new murmurs after trauma
• Most operated on
• Small septal defects may be treated conservatively

Coronary artery injury

• Rare in blunt trauma. Includes AV fistulas, dissection, thrombosus and laceration
• LAD most commonly involved
• Presents as MI in same territory
• Treated by PCI with stenting and has a more favourable prognosis than atherosclerotic MI
• Fibrinolytic therapy is contraindicated
• Must take extreme caution in subsequent antiplatelet and anticoagulant therapy due to concomitant injuries

Cardiac rupture

• Splashing mill wheel sounding murmur (bruit de Moulin) if survive to hospital
• Mostly RV due to anterior and thinner walled
• ECG may show conduction defects or axis deviation if herniation has occurred
• Diagnosis by USS is necessary
• Immediate thoracotomy necessary for survival

Presentation of cardiac injury

• Chest pain (all types), SOB, palpitations, dizziness
• Careful attributing all chest pain to wall structures
• Unexplained tachycardia is often the key to raise suspicions
• Myocardial contusion
  • Chest pain, pericardial rub, S3, cardiac failure
  • ST/T wave changes anteriorly, heart blocks, incomplete RBBB, inferior Q waves
  • Echo: RWMA
  • Tn elevation

ECG

• NPV of normal ECG is 80-90% but not good enough in isolation
• Significant events can occur up to 24 hours after injury
• More sensitive for left-sided injury than right
• Non-specific sinus tachycardia and ST-T wave changes are not predictive of blunt cardiac injury
• A small subset will have ECG findings consistent with MI
  • Consider coronary artery disease or acute coronary artery dissection with thrombosis formation over 5-7 days after injury
• If normal ECG but suspicion remains, monitor for 4-6 hours and repeat ECG
  • Can be safely discharged if this remains normal
• If ECG abnormal but stable, admit for monitoring with serial ECG’s

ECG monitoring

• Indications
  • Previous history of IHD or AF
  • Transmural MI pattern on ECG
  • Haemodynamically significant arrhythmias
• Not required in:
  • Non-specific ST/T wave change
  • Elevated cardiac biomarkers (if done)
• Nearly all patients at risk of significant arrhythmias will be monitored for other injuries anyway

Troponin

• Sensitivity 12-23% and specificity 97-100%
• One study showed normal presenting ECG with normal troponin at presentation and at 6 hours had no clinically significant blunt cardiac injury
• Sensitivity of an abnormal ECG with elevated troponin for clinically significant blunt cardiac trauma was 100% with PPV of 62%
• Increased troponin at presentation or within 6 hours is associated with increased risk of dysrhythmia and decreased ejection fraction
• UTD states:
  • Not routinely done unless haemodynamically unstable, signs of severe trauma or ECG with significant abnormalities
    • If one or more of these do exist, or >60yo, it is done at presentation and at 6 hours. If normal, still do echo workup. If raised, the level of elevation may be prognostic
  • In lieu of this, authors use repeated examination, serial ECG and cardiac monitoring for 4-6 hours to screen for BCI
    • Biomarkers have not been shown to be better than this approach

Echocardiogram

• Helpful if signs of BCI but contributes little if haemodynamically stable without arrhythmia
• Recommended (UTD) to get one if blunt thoracic trauma with unexplained hypotension or any symptoms/signs consistent with BCI
• POCUS has sensitivity of 100% and specificity of 99% for pericardial effusion
• TOE is 3x more sensitive for blunt cardiac injury than TTE
• Recommended in all patients with elevated troponin, dysrhythmias, unexplained hypotension, CCF, or myocardial dysfunction

Treatment of blunt cardiac injury

• Treat hypovolaemia with crystalloids or blood products preferably
  • Hypotension usually due to hypovolaemia vs. cardiac dysfunction
  • If euvolaemic, add inotropes
• Moderate to high risk patients (abnormal ECG, raised troponin, associated injuries, dysrhythmias, failure symptoms) should have troponin and echo
• Admission for ward telemetry over 24-48 hours is appropriate for patient with minor ECG abnormalities (PAC’s or PVC’s), no significant concomitant injuries and normal haemodynamics
• Urgent surgery if cardiac rupture, valvular injury, papillary muscle/chordae tendinae rupture
• Urgent PCI if coronary thrombosus or dissection

Pericardial inflammation syndrome

• Can arise due to delayed hypersensitivity reaction to damaged myocardium in the pericardial cavity
• Must consider if chest pain, fever and pleural/pericardial effusions 2-4 weeks after cardiac trauma or surgery
• May have friction rubs, arthralgias and pulmonary infiltrates
• ECG often diagnostic of pericarditis
• NSAID’s and rest usually control symptoms by 12-24 hours
• Steroids and/or drainage of pleural or pericardial effusion is sometimes required

Thoracic great vessels

• Includes
  • Aorta
  • Brachiocephalic trunk – Right subclavian and right common carotid
  • Left subclavian
  • Left common carotid
  • Pulmonary artery and branches
  • Superior and inferior vena cavae
  • Innominate and azygos veins
• Exsanguinating haemorrhage is the primary acute concern
• Injury can also lead to aneurysm and pseudoaneurysm formation with subsequent fistula formation and massive haemorrhage
• Most have suffered penetrating trauma with dire prognosis
• Most die before reaching hospital
• Aortic injuries are usually due to MVA – 90% die at scene, further 5% within 24 hours and a further 4% over the next 4 months = 1% survival rate over 4 months
• Mortality for untreated patients is 1% per hour for the initial 48 hours

• Aortic blunt injury
  • Deceleration forces most common. Also compression between sternum and spine can cause this
  • Consider blunt aortic injury if fall 3m or MVA >50km/hr
  • Proximal descending aorta most common site of blunt trauma due to fixation of vessels between left subclavian and ligamentum arteriosum leading to shearing forces
  • Ascending aortic injury is rarely diagnosed as die at scene and associated with cardiac rupture, severe myocardial contusion and multiple tears
  • Distal descending aorta can also rarely be injured presenting with paraplegia, mesenteric ischaemia, anuria or lower extremity ischaemia
    • The more distal the injury, the better the prognosis
  • 85% primarily involve aorta
  • Branch vessel injuries in 15%

• Subclavian artery
  • Usually direct trauma to distal portion with intimal damage and occlusion associated with first rib and clavicular fractures
  • Occasionally avulsed at origin
• Innominate artery
  • Second only to injury at the aorta
  • <50% of patients have symptoms (may be subtle reduced right radial pulse, systolic murmur or distal ischaemia –rarely)
• Pulmonic veins and vena cavae
  • Attach to atria and can shear there
  • Venous thoracic great vessel injury is extremely rare and most fatal

• Penetrating injury
  • Rarely reach hospital
  • Missiles may embolise to areas distant from entry point or, if in chest, may fall to most dependent portion i.e. posterior costophrenic recess

• Presentation
  • Any high energy mechanism can cause injury
  • Side-impact and head-on of equal likelihood
  • 50% of patients present without external physical signs of injury
  • Clues
    • Hypotension
    • Hypertension in upper extremities with hypotension in lower extremities, unequal blood pressures
    • Seatbelt sign, steering wheel contusion on chest wall
    • Thoracic outlet expanding haematoma
    • Intrascapular murmurs/bruits
    • Palpable sternal/rib fractures and flail chest
• Remember to perform full neurological examination in case of spinal artery involvement

• Diagnosis
  • CXR
    • Widened mediastinum >8cm or ratio 0.38
      • Normal mediastinal width DOES NOT rule out aortic injury (95% sensitive if <65)
      • 80% sensitive for all ages and 80% specific for all ages
      • Supine CXR 90% sensitive, erect CXR 95% sensitive)
    • One sensitive sign is deviation of the oesophagus >1cm to the right of the spinous process at T4
    • See next slide
  • New murmur 93% specific but very insensitive
  • Haemothorax 88% specific but very insensitive
  • First/second rib fracture 73% specific but very insensitive
  • CT angiography
    • Diagnostic modality of choice

• CXR signs suggestive of great vessel injury
  • Fractures – Sternum, ribs, clavicles in multitrauma, first rib, scapula
  • Mediastinal
    • Obliteration of aortic knob contour
    • Widened >8cm or >0.38 ratio
    • Depression of left mainstem bronchus >140 degrees
    • Loss of paravertebral pleural stripe
    • Calcium layering at aortic knob
    • Abnormal general appearance
    • Deviation of NG tube to the right at T4 >1cm from spinous process
    • Lateral displacement of trachea
    • Loss of aortopulmonary window
  • Apical pleural haematoma (cap)
    • This is extrapleural blood from mediastinal haematoma, thoracic spine #, great vessel injury, 1st rib/clavicle # or scapula #
  • Massive left haemothorax
  • Obvious diaphragmatic injury

• CT signs of traumatic aortic injury
  • Aortic pseudoaneurysm
  • Periaortic haemorrhage
    • Fat around the vessels becomes obliterated and infiltrated with streaky soft tissue density = blood
  • Displacement of trachea and oesphagus to right
  • Irregular shape of aortic lumen
  • Intimal flaps
  • Luminal clots at sites of intimal disruption
  • Sudden coarctation
  • Small aortic calibre in lower chest and abdomen
  • Peridiaphragmatic haemorrhage (from proximal intraluminal thrombus)
  • Transection of the aorta
  • Active from bleeding aorta into mediastinum

• Transoesophageal echocardiography
  • Can be done at bedside of unstable patient with aortic rupture
  • Diagnoses intimal lesions often missed by other modalities
  • Contraindicated if suspected C-spine injuries or airway difficulties
• Aortography
  • Useful if CT results indeterminate
• Treatment
  • Initial management involves anti-impulse therapy for patients with SBP >100 with beta-blockers +- vasodilators (see below)
  • Management then depends on grade of injury
    • Grade I: Intimal tear -> Non-operative management with aggressive anti-impulse therapy and serial imaging
    • Grade II: Intramural haematoma
    • Grade III: Pseudoaneurysm
    • Grade IV: Rupture (periaortic haematoma/free rupture)
    • Grades II/III/IV -> Repair indicated
  • EAST guideline
    • Minimal aortic injury is described as <10mm intimal flap with no haematoma or pseudoaneurysm -> Conservatively managed with BP control
    • Anything else is major and requires repair after life threats
  • Repair is ideally delayed and endovascular but depends on haemodynamic stability
    • Endovascular contraindicated if aorta is tiny (<15mm calibre) or tear of mid-arch
    • All penetrating injuries need washout but can be done separately to endovascular repair if required
    • Endovascular has less risk of paraplegia, mortality, blood loss and equal stroke risk
  • Pharmacological control of BP and HR are paramount if any delay in transport
    • Target SBP 100-120 and HR around 60
    • Bisoprolol infusion for HR control, then bring in vasodilator (e.g. sodium nitroprusside) for further BP control
    • Narcotics also helpful for BP control
    • Decreasing the slope of the dP/dT (change in pressure/change in time) will decrease wall tension and shearing forces

Last Updated on May 14, 2024 by Andrew Crofton